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61,005 resultsShowing papers similar to Polystyrene nanoplastics exacerbate dibutyl phthalate-induced liver fibrosis through PDGFRα-dependent hepatic stellate cell activation
ClearPolystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.
Polystyrene nanoplastics exacerbated Pb-induced liver toxicity in mice
Researchers found that polystyrene nanoplastics exacerbated lead-induced liver toxicity in mice, with co-exposure causing higher lead accumulation, more severe inflammation, increased oxidative stress, and greater disruption of protective Nrf2 signaling pathways compared to lead alone.
Accumulation of polystyrene microplastics induces liver fibrosis by activating cGAS/STING pathway
Researchers found that tiny polystyrene microplastics (0.1 micrometers) can enter liver cells and cause DNA damage that triggers a chain reaction leading to liver scarring, known as fibrosis. The microplastics activated a specific immune signaling pathway called cGAS/STING, which caused inflammation that progressively damaged liver tissue even at low concentrations. This study reveals a specific mechanism by which long-term microplastic exposure could lead to serious liver disease in humans.
Exposure to Di(2‐Ethylhexyl) Phthalate Increases the Internalization of Polystyrene Microplastics by Human Hepatocellular Carcinoma Cells and Leads to Cell Damage
Researchers found that the common plasticizer DEHP significantly increased the uptake of polystyrene microplastics by human liver cancer cells in laboratory experiments. The smallest microplastic particles (100 nanometers) had the highest uptake rate, and DEHP exposure boosted internalization especially for the larger particles. The study raises concerns that co-exposure to plasticizers and microplastics, which commonly occur together in the environment, could amplify cellular damage beyond what either pollutant causes alone.
Adverse Effect of Polystyrene Nanoplastics in Impairing Glucose Metabolism in Liver Injury
Polystyrene nanoplastics disrupted glucose metabolism in liver cells by interfering with insulin signaling pathways and mitochondrial function, suggesting that nanoplastic exposure could contribute to metabolic disorders including insulin resistance.
Polystyrene Nanoplastics Exacerbate HFD-induced MASLD by Reducing Cathepsin Activity and Triggering Large Vacuole Formation via Impaired Lysosomal Acidification
Researchers found that polystyrene nanoplastics, when combined with a high-fat diet in mice, significantly worsened fatty liver disease symptoms compared to either factor alone. The nanoplastics impaired the function of lysosomes, the cell's recycling centers, by preventing proper acidification and reducing enzyme activity. The study suggests that nanoplastic exposure could amplify diet-related liver problems by interfering with how cells process and break down fats.
[Exposure Pathways of Polystyrene Nanoplastics Mediate Their Cellular Distribution and Toxicity].
This study found that the route by which polystyrene nanoplastics enter the body determines which liver cell types accumulate the particles and what toxic effects occur, demonstrating that exposure pathway—not just dose—shapes nanoplastic toxicity in hepatic tissue.
Dietary exposure to polystyrene microplastics exacerbates liver damage in fulminant hepatic failure via ROS production and neutrophil extracellular trap formation
In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
The mechanism of polystyrene nanoplastics hepatotoxicity in zebrafish (Danio rerio)
This study investigated the hepatotoxic mechanisms of polystyrene nanoplastics in zebrafish (Danio rerio), finding that nanoplastics accumulating in the liver triggered oxidative stress and cellular injury pathways. The results highlight nanoplastics as a significant liver toxicant in aquatic vertebrates.
Co-Exposure to Polystyrene Microplastics and Bisphenol A Contributes to the Formation of Liver Fibrosis in Mice through Inhibition of the BMAL1/E-Cad Signaling Pathway
Researchers found that co-exposure to polystyrene microplastics and bisphenol A caused liver fibrosis in mice by disrupting a key signaling pathway that controls cell adhesion. The combined exposure produced more severe liver damage than either substance alone, with excessive buildup of scar tissue in the liver. The study suggests that the widespread co-occurrence of microplastics and BPA in food packaging could pose synergistic risks to liver health.
FGFR2-regulated cytoskeletal rearrangement disturbs autophagy flux induced by polystyrene nanoplastics
Researchers found that polystyrene nanoparticles activate the cell-surface receptor FGFR2 in liver cells, triggering cytoskeletal rearrangement that blocks the normal autophagy pathway — the cell's waste-removal system — leading to mitochondrial and lysosomal dysfunction and identifying a previously unknown molecular mechanism for nanoplastic cellular toxicity.
Environmentally relevant UV-light weathering of polystyrene micro- and nanoplastics promotes hepatotoxicity in a human cell line
Researchers found that UV-weathered polystyrene micro- and nanoplastics at environmentally relevant concentrations induced hepatotoxicity in human liver cells and caused significant changes in gene expression related to liver disease pathways.
PS-MPs Induced Inflammation and Phosphorylation of Inflammatory Signalling Pathways in Liver
Polystyrene microplastics (0.1 µm) induced inflammatory responses and activated multiple inflammatory signalling pathways in mouse and human liver cell lines after 28 days of exposure. The study identified specific phosphorylation cascades through which PS MPs trigger hepatic inflammation, linking microplastic exposure to liver damage mechanisms.
Polystyrene microplastics-induced macrophage extracellular traps contributes to liver fibrotic injury by activating ROS/TGF-β/Smad2/3 signaling axis
In a mouse study, polystyrene microplastics caused liver scarring (fibrosis) by triggering immune cells called macrophages to release web-like traps that promoted inflammation. Smaller microplastic particles caused more severe liver damage than larger ones, and the damage involved a specific signaling pathway (ROS/TGF-beta/Smad2/3) that drives tissue scarring. This research reveals a new mechanism by which microplastics may contribute to chronic liver disease.
Polystyrene nanoplastics induce intestinal and hepatic inflammation through activation of NF-κB/NLRP3 pathways and related gut-liver axis in mice
In a mouse study, ingested polystyrene nanoplastics accumulated in the gut and liver and triggered inflammation through specific immune pathways, damaging the intestinal lining and allowing bacterial toxins to leak into the liver. This gut-liver connection suggests that swallowing nanoplastics could set off a chain reaction of inflammation affecting multiple organs in the body.
Exposure to polystyrene nanoplastics induces hepatotoxicity involving NRF2-NLRP3 signaling pathway in mice
Mice and liver cells exposed to 20-nanometer polystyrene nanoplastics developed liver damage through a specific molecular pathway involving oxidative stress and inflammation. The study showed that activating the body's natural antioxidant defense system (called NRF2) could protect against this liver injury, offering a potential avenue for reducing nanoplastic-related harm to human liver health.
Exposure to Polyethylene Terephthalate Microplastic Induces Mouse Liver Fibrosis Through Oxidative Stress and p38 MAPK/p65 NF‐κB Signaling Pathway
Researchers found that exposure to PET microplastics induced liver fibrosis in mice through oxidative stress and activation of the p38 MAPK/p65 NF-kB signaling pathway. The study suggests that PET microplastics, which are frequently detected in both environmental samples and human tissues, may contribute to liver damage through inflammatory and oxidative mechanisms.
Polystyrene nanoplastics exacerbate lipopolysaccharide-induced myocardial fibrosis and autophagy in mice via ROS/TGF-β1/Smad
Researchers found that polystyrene nanoplastics worsened heart damage in mice already exposed to bacterial toxins, accelerating scarring and disrupting normal heart tissue maintenance. The combined exposure triggered increased oxidative stress and activated a specific signaling pathway linked to tissue fibrosis. The study suggests that nanoplastic exposure could amplify existing cardiac stress, potentially compounding heart problems when the body is already under inflammatory challenge.
Effects of polystyrene micro/nanoplastics on liver cells based on particle size, surface functionalization, concentration and exposure period
Researchers systematically studied the effects of polystyrene micro- and nanoplastics on human liver cells, varying particle size, surface chemistry, concentration, and exposure duration. They found that smaller particles were internalized more readily and that surface functionalization significantly influenced toxicity, with aminated particles causing the most cell damage. The study suggests that particle characteristics beyond just size play an important role in determining how micro- and nanoplastics affect human cells.
The combined toxicity of polystyrene nano/micro-plastics and triphenyl phosphate (TPHP) on HepG2 cells
This study found that polystyrene nanoplastics and microplastics made a common flame retardant chemical (TPHP) more toxic to human liver cells than the chemical alone. The nanoplastics absorbed the flame retardant and delivered it to cells, causing increased oxidative stress, mitochondrial damage, and cell death. Smaller nanoplastics caused more harm than larger microplastics, suggesting that as plastics break down into smaller pieces, their ability to carry toxic chemicals into human cells increases.
Polystyrene Nanoplastics Induce Pyroptosis in HepG2 Cells via the YAP1-cGAS-STING Signaling Axis.
Scientists found that tiny plastic particles from polystyrene (commonly used in disposable cups and food containers) can trigger a harmful type of cell death in liver cells. When these microscopic plastic pieces enter liver cells, they activate a specific pathway that causes the cells to essentially self-destruct, which could potentially damage the liver over time. This research helps explain how the plastic pollution we're exposed to daily might be harming our bodies, particularly our liver health.
Polystyrene microplastics induce hepatic lipid metabolism and energy disorder by upregulating the NR4A1-AMPK signaling pathway
Researchers found that polystyrene microplastics accumulate in the liver and disrupt fat and energy metabolism by activating a specific molecular pathway called NR4A1-AMPK. This activation triggers a self-cleaning process called autophagy that reduces fat production in liver cells, while also increasing harmful reactive oxygen species. The findings suggest that long-term microplastic exposure could lead to ongoing liver damage through this metabolic disruption.
Hepatotoxic of polystyrene microplastics in aged mice: Focus on the role of gastrointestinal transformation and AMPK/FoxO pathway
This study found that polystyrene microplastics caused liver damage in aged mice, with the particles undergoing chemical changes as they passed through the digestive system that may have made them more harmful. The microplastics disrupted key metabolic pathways in the liver, triggered inflammation, and caused DNA damage through oxidative stress. The findings are especially concerning because older individuals may be more vulnerable to the liver-damaging effects of microplastic exposure.
Enhanced hepatic cytotoxicity of chemically transformed polystyrene microplastics by simulated gastric fluid
Polystyrene microplastics transformed by simulated gastric fluid showed significantly increased cytotoxicity in hepatocytes compared to untransformed MPs, suggesting that digestive bioprocessing alters the surface chemistry of ingested microplastics in ways that heighten their liver toxicity.